The metastasis‐associated protein‐1 gene encodes a host permissive factor for schistosomiasis, a leading global cause of inflammation and cancer

Sujit S. Nair, Anitha Bommana, Jeffrey M. Bethony, Amanda J. Lyon, Kazufumi Ohshiro, Suresh B. Pakala, Gabriel Rinaldi, Brian Keegan, Sutas Suttiprapa, Maria V. Periago, Peter J. Hotez, Paul J. Brindley, Rakesh Kumar – 12 April 2011 – Schistosoma haematobium is responsible for two‐thirds of the world's 200 million to 400 million cases of human schistosomiasis. It is a group 1 carcinogen and a leading cause of bladder cancer that occurs after years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells

Timea Csak, Michal Ganz, Justin Pespisa, Karen Kodys, Angela Dolganiuc, Gyongyi Szabo – 12 April 2011 – The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome activation involves sequential hits. The inflammasome, which cleaves pro–interleukin‐1β (pro–IL‐1β) into secreted IL‐1β, is induced by endogenous and exogenous danger signals. Lipopolysaccharide (LPS), a toll‐like receptor 4 ligand, plays a role in NASH and also activates the inflammasome.

Antiviral activity of the hepatitis C virus polymerase inhibitor filibuvir in genotype 1–infected patients

Frank Wagner, Robert Thompson, Constantino Kantaridis, Paul Simpson, Philip J. F. Troke, Shyla Jagannatha, Srividya Neelakantan, Vivek S. Purohit, Jennifer L. Hammond – 12 April 2011 – More effective and better‐tolerated therapies are needed for chronic hepatitis C virus (HCV) infection. Among the direct‐acting anti‐HCV agents in development is the nonstructural 5B protein (NS5B polymerase) non‐nucleoside inhibitor filibuvir.

Serum and liver iron differently regulate the bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway in mice

Elena Corradini, Delphine Meynard, Qifang Wu, Shan Chen, Paolo Ventura, Antonello Pietrangelo, Jodie L. Babitt – 12 April 2011 – The bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway is a central regulator of hepcidin expression and systemic iron balance. However, the molecular mechanisms by which iron is sensed to regulate BMP6‐SMAD signaling and hepcidin expression are unknown. Here we examined the effects of circulating and tissue iron on Bmp6‐Smad pathway activation and hepcidin expression in vivo after acute and chronic enteral iron administration in mice.

Murine hepatic stellate cells veto CD8 T cell activation by a CD54‐dependent mechanism

Frank A. Schildberg, Alexandra Wojtalla, Sören V. Siegmund, Elmar Endl, Linda Diehl, Zeinab Abdullah, Christian Kurts, Percy A. Knolle – 12 April 2011 – The liver has a role in T cell tolerance induction, which is mainly achieved through the functions of tolerogenic hepatic antigen‐presenting cells (APCs) and regulatory T cells. Hepatic stellate cells (HSCs) are known to have various immune functions, which range from immunogenic antigen presentation to the induction of T cell apoptosis. Here we report a novel role for stellate cells in vetoing the priming of naive CD8 T cells.

Epithelial cell specificity and apotope recognition by serum autoantibodies in primary biliary cirrhosis

Guanghua Rong, Renqian Zhong, Ana Lleo, Patrick S.C. Leung, Christopher L. Bowlus, Guo‐Xiang Yang, Chen‐Yen Yang, Ross L. Coppel, Aftab A. Ansari, Dean A. Cuebas, Howard J. Worman, Pietro Invernizzi, Gregory J. Gores, Gary Norman, Xiao‐Song He, M. Eric Gershwin – 12 April 2011 – A major enigma of primary biliary cirrhosis (PBC) is the selective targeting of biliary cells.

Fatty liver index and mortality: The cremona study in the 15th year of follow‐up

Giliola Calori, Guido Lattuada, Francesca Ragogna, Maria Paola Garancini, Paolo Crosignani, Marco Villa, Emanuele Bosi, Giacomo Ruotolo, Lorenzo Piemonti, Gianluca Perseghin – 12 April 2011 – A fatty liver, which is a common feature in insulin‐resistant states, can lead to chronic liver disease. It has been hypothesized that a fatty liver can also increase the rates of non–hepatic‐related morbidity and mortality.

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